DNA Oxidative Damage is Correlated with JNK Activation in Hepatocytes from Rats with Experimental Insulin ResistanceZagayko AL*, Kravchenko GB, Krasilnikova OA and KochubeyJu I
Department of Biochemistry, National National University of Pharmacy Kharkiv, Kharkiv 61068, Ukraine
- Corresponding Author:
- Zagayko Andrey L
Department of Biochemistry
National University of Pharmacy Kharkiv, Kharkiv 61068, Ukraine
E-mail: [email protected]
Received date: December 18, 2013; Accepted date: February 25, 2014; Published date: March 03, 2014
Citation: Zagayko AL, Kravchenko GB, Krasilnikova OA, Ju KI (2014) DNA Oxidative Damage is Correlated with JNK Activation in Hepatocytes from Rats with Experimental Insulin Resistance. J Mol Genet Med S1:023. doi: 10.4172/1747-0862.S1-023
Copyright: © 2014 Zagayko AL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Oxidative stress was improved as the main complication for a variety of pathological conditions. The present study was aimed to investigate the effect of insulin resistance development on c-Jun-N-terminal kinases (JNK) activity and DNA/RNA oxidative damage in rat’s liver under fructose rich diet. Total JNK, phosphorylated JNK-1 and JNK-2 ([pThr183/Tyr185] c-Jun N-terminal protein kinase (pJNK1/2), and 8-hydroxy-2`-deoxyguanosine (8-OHdG) amounts were measured in hepatocyte lysate. Glucose, insulin, free fatty acids, and triacylglicerols concentration and thiobarbituric acid reactive substances concentrations were measured in blood plasma. Catalase and superoxide dismutase activity, and thiobarbituric acid reactive substances (TBARS) were determined in liver homogenate. Fructose rich diet in rats provoked the insulin resistance that is accompanied by deep metabolic abnormalities detected in our study. These metabolic abnormalities induced by fructose overload are associated with an enhanced oxidative stress which appears to deregulate the JNK pathway. Consequently, accumulation of DNA/RNA oxidative damage stress marker – 8-OHdG– in hepatocytes positively correlates with JNK activity in the cells.